Protein power A protein that could be harnessed to prevent or reverse the onset of type 1 diabetes has been identified by Australian researchers.

The researchers found the protein - CD52 - plays a key role in protecting the body against excessive immune responses, and could be used to treat other autoimmune disorders such as multiple sclerosis and rheumatoid arthritis.

Study leader, Professor Len Harrison, of the Walter and Eliza Hall Institute, says the team has already found CD52 prevents type 1 diabetes in mouse models and is confident of moving "quickly to clinical trials".

The findings, published today in Nature Immunology, focuses on the role CD52 plays in suppressing the body's immune response to the specific antigens that drive autoimmune disease.

Autoimmune diseases, such as type 1 diabetes, develop when the immune system begins to attack the body's own tissues.

The protein CD52 appears to play a dominant role in controlling or suppressing immune activity in the early stages of the immune response, Harrison says.

Harrison and colleagues' findings follow on from their earlier discovery T cells, specialised immune cells, that regulate the activity of other T cells.

Harrison says this latest paper outlines the mechanism by which these regulatory T cells work.

Works like a brake

The researchers found T cells that carry high levels of CD52 release the CD52 to "dampen down or put a brake on" the growth of T cells being activated by the disease-causing antigens.

Harrison says their work shows people with type 1 diabetes are less able to generate CD52 cells and therefore lose this protection.

They were able to demonstrate the link with the onset of the autoimmune disease as the removal of the CD52-producing immune cells in mouse models led to the rapid development of diabetes.

"The data we have so far indicates CD52 is an effective immune-suppressing agent so we are excited about its therapeutic potential," says Harrison.

The discovery of the protective mechanism could also provide a tool to identify people at risk of developing autoimmune diseases.

Harrison says he and colleagues have been able to measure a deficiency of this mechanism in laboratory tests and hope to ultimately screen for CD52 deficiency to pinpoint people at risk of specific autoimmune diseases.

He says boosting the levels of CD52 in people at risk may be one approach to developing a treatment for diabetes.